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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
Published on: June 25, 2014
Cytokine-induced functional suppression of microencapsulated rat pancreatic islets in vitro
A King1, A Andersson, S Sandler
1Department of Medical Cell Biology, Biomedicum, Uppsala University, Sweden. aileen.king@medcellbiol.uu.SE
Insights
Alginate/poly-L-lysine/alginate microencapsulation does not protect islets from inflammatory cytokines like interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Microencapsulated islets showed increased susceptibility to IL-1β, but recovery was observed at lower concentrations.
Area of Science:
- Biomedical Engineering
- Immunology
- Endocrinology
Background:
- Inflammatory cytokines are likely released near microencapsulated islets in vivo.
- Assessing the impact of these cytokines on islet function is crucial for transplantation success.
Purpose of the Study:
- To investigate the effects of interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) on microencapsulated rat islets.
- To determine if microencapsulation protects islets from cytokine-induced suppression and to assess their recovery.
Main Methods:
- Microencapsulated rat islets were cultured with IL-1β and TNF-α.
- Insulin release and glucose oxidation rates were measured.
- The recovery of islets from IL-1β-induced suppression was evaluated.
Main Results:
- Microencapsulated islets showed suppression upon exposure to IL-1β, potentiated by TNF-α.
- At higher IL-1β concentrations, microencapsulated islets were more suppressed than nonencapsulated islets.
- Both microencapsulated and control islets recovered from suppression at lower IL-1β concentrations (2.5 U/ml).
Conclusions:
- Alginate/poly-L-lysine/alginate microencapsulation does not protect islets against IL-1β and TNF-α.
- Microencapsulated islets appear more susceptible to IL-1β-induced suppression at higher concentrations.
- Recovery from IL-1β exposure is possible at lower concentrations.
Background:
It is likely that inflammatory cytokines are released near microencapsulated islets in vivo.
Methods:
Rates of insulin release or glucose oxidation were measured after culture of microencapsulated rat islets with interleukin (IL)-1beta and tumor necrosis factor-(TNF-alpha). Their ability to recover from IL-1beta-induced suppression was also investigated.
Results:
Microencapsulated islets were suppressed after exposure to IL-1beta, which was potentiated by TNF-alpha. After exposure to lower IL-1beta concentrations, microencapsulated islets had similar oxidation rates as corresponding controls. At higher concentrations, microencapsulated islets were more suppressed than nonencapsulated islets. Microencapsulated and control islets were able to recover from suppression after exposure to 2.5 U/ml of IL-1beta.
Conclusions:
Microencapsulation using the present alginate/poly-L-lysine/alginate capsules does not protect islets against the detrimental effects of IL-1beta and TNF-alpha. Indeed, microencapsulated islets seem to be more susceptible to suppression at higher concentrations of IL-1beta. However, after exposure to a lower concentration of IL-1beta, microencapsulated islets can recover.

